Studies have shown that JNK1/2 is involved in the sensitization of p38-MAPK inhibition to cisplatin-induced cell death, and the elevated level of reactive oxygen species (ROS) mediates the activation of JNK1/2 by P38-MAPK inhibition.80 Compared to wild-type controls, JNK1 knockout mice showed a significant decrease in gastric carcinogenesis mediated by N-methyl-N-nitrosourea.81 Consequently, JNK1 is involved in tumor initiation as well as progression and is a promising target for the prevention of GC. Here, MAPK8 is linked to gastric cancer.